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sepsis in patients, allowing differentiation between patients with systemic inflammatory response syndrome and patients with sepsis ( Yousef et al . 2010 ). The hypothalamic–pituitary–adrenal (HPA) axis plays an important protective role in the body

Introduction The classic response to chronic stress consists of an elegant, concerted interplay of two important pathways, the sympathetic nervous system (SNS) and the hypothalamus–pituitary–adrenal axis (HPA). The chronic activation of these stress

Introduction Adaptation to stress is a basic phenomenon in mammalian life that is mandatorily associated with the activity of the hypothalamic–pituitary–adrenal (HPA) axis. Extracellular signaling molecules that stimulate the HPA axis at the brain

). Hyperactivity of the HPA axis is positively correlated with the metabolic syndrome, suggesting a causative role for GCs in the obese phenotype ( Vegiopoulos & Herzig 2007 ). Indeed, Cushing’s patients are characterized by a redistribution of body fat from the

stress induces release of glucocorticoids (GCs) (mainly cortisol in humans and corticosterone in rodents) from the adrenal gland to adapt energy metabolism to a perceived fight-or-flight situation. HPA axis activation is initiated by an increase in

–pituitary–adrenal (HPA) axis, which controls the plasma levels of glucocorticoids, establishes healthy metabolic function and stress responsivity later in life, and this is influenced by diverse stimuli including maternal care, diet, immune challenge, and stress ( Maniam

Introduction The early environment of the embryo, foetus and newborn have been clearly linked to altered hypothalamic–pituitary–adrenal (HPA) function and related behaviours through the juvenile period and into adulthood (for reviews see

( de Kloet et al. 2005 , Joëls 2018 ). The maintenance of homeostasis by GCs is tightly regulated by hypothalamus–pituitary–adrenal (HPA) axis activity ( Lightman et al. 2020 ). The hypothalamic neurons from the paraventricular nucleus release the

expressed in the pancreatic islets from MSG-obese rats ( Miranda et al . 2014 ). However, in addition to PNS hyperactivity, dysfunction in the hypothalamus–pituitary–adrenal (HPA) axis is an important factor that contributes to metabolic syndrome ( Wang

( Anagnostis et al . 2009 ). Production of endogenous glucocorticoids is regulated by the maternal hypothalamic–pituitary–adrenal (HPA) axis. Stress triggers the hypothalamus to produce corticotropin-releasing hormone (CRH), which is secreted into the